Human violent behavior is a complex behavior which is influenced by genetic and environmental factors. There is a trend in investigating the mechanism of violent behavior by using the genetic methods. This article reviews several candidate genes and advances in epigenetics which are associated with violent behavior. The prospects and significance of violent behavior research from the view of gene polymorphism and epigenetics are also discussed.
Aggression ; Epigenesis, Genetic ; Forensic Genetics ; Humans ; Polymorphism, Genetic ; Violence

To study the effect of Gegen Qinlian decoction and its major effective components on five hepatic microsomal CYP450 isozymes in rats. The in vitro hepatic microsomal incubation technique was used to co-culture Gegen Qinlian decoction and its major effective components together with each probe substrate. HPLC-MS/MS was used to establish the analytical method for metabolites of the five isoform probe substrates of CYP450 isozymes, detect the linearity among micoromal protein concentration, incubation time and metabolite formation amount. And HPLC-MS/MS was applied to determine the formation rate (V) of corresponding metabolites (acetaminophen, 4-OH-chlorzoxazone, dextrophan, 6-OH-chlorzoxazone and 6β-hydroxytestosterone) specific probe substrates of the five isoform probe substrates of CYP450 isozymes (phenacetin, polbutamide, dextromethorphan, chlorzoxazone, testosterone), in order to determine the activity of each isozyme. The result showed good linearity among acetaminophen, 4-OH-tolbutamide, dextrophan, 6-OH-chlorzoxazone and 6β-hydroxytestosterone, satisfactory precision, stability and average recovery, suggesting the method was feasible. The optimized in vitro microsomal incubation conditions conformed to the requirements in the guideline of drug-drug interaction. Gegen Qinlian decoction showed different degrees of inhibitor effect on 5 CYP450 isoforms (CYP1A2, CYP2C11, CYP2D2, CYP2E1, CYP3A1/2). Its major effective component berberine could inhibit each CYP450 isoform at high concentrations (except for CYP1A2, CYP3A1/2).
Animals ; Chromatography, High Pressure Liquid ; methods ; Cytochrome P-450 Enzyme Inhibitors ; pharmacology ; Drugs, Chinese Herbal ; pharmacology ; Isoenzymes ; antagonists & inhibitors ; Liver ; enzymology ; Rats ; Tandem Mass Spectrometry ; methods

Objective: To uncover the underlying mechanisms of action of the Yinlai decoction on high-calorie diet-induced pneumonia through proteomics analysis. Methods: Based on the Gene Expression Omnibus (GEO) database, lung tissue samples from normal and high-fat diet (HFD) fed mice in the GSE16377 dataset were selected as test cohorts to identify differentially expressed genes and conduct bioinformatics analyses. In the animal experiments, mice were randomly divided into the control (N), high-calorie diet pneumonia (M), and Yinlai decoction treatment (Y) groups. Mice in the M group received high-calorie feed and a 0.5 mg/mL lipopolysaccharide solution spray for 30 min for 3 d. The mice in the Y group were intragastrically administered 2 mL/10 g Yinlai decoction twice daily for 3 d. Pathological evaluation of the lung tissue was performed. Differentially expressed proteins (DEPs) in the lung tissue were identified using quantitative proteomics and bioinformatics analyses. The drug-target relationships between Yinlai decoction and core DEPs in the lung tissue were verified using AutoDock Vina and Molecular Graphics Laboratory (MGL) Tools. DEPs were verified by western blot. Results: GEO data mining showed that an HFD altered oxidative phosphorylation in mouse lung tissue. The Yinlai decoction alleviated pathological damage to lung tissue and pneumonia in mice that were fed a high-calorie diet. A total of 47 DEPs were identified between the Y and M groups. Enrichment analysis revealed their association with energy metabolism pathways such as the tricarboxylic acid cycle (TCA) and oxidative phosphorylation. The protein-protein interaction network revealed that Atp5a1, Pdha1, and Sdha were the target proteins mediating the therapeutic effects of Yinlai decoction. Molecular docking results suggested that the mechanism of the therapeutic effect of Yinlai decoction involves the binding of brassinolide, praeruptorin B, chrysoeriol, and other components in Yinlai decoction to Atp5a1. Conclusion The Yinlai decoction alleviated lung tissue damage and pneumonia in mice that were fed a high-calorie diet by regulating the TCA and oxidative phosphorylation. Our study highlights the importance of a healthy diet for patients with pneumonia and provides a scientific basis for the prevention and treatment of pneumonia through dietary adjustments.

An information system for "Internet+" hierarchical diagnosis and treatment was constructed with pa-tients as its center,with clinical information system as its basis,and with solution of difficulties in implementation of "Internet+" hierarchical diagnosis and treatment as its guidance. Its three key modules, namely online service module,data center module and off-line management module,were designed and analyzed,which helps the preci-sion match of resources and demands for the"Internet+" hierarchical diagnosis and treatment,promotes the vertical flow of good medical resources and improves the grass-root service level and efficiency.

This study was aimed to investigate the effect of chemokine-like factor superfamily 8 (CKLFSF8) on proliferation and expression of epidermal growth factor receptor (EGFR) of HL-60 cells. Expression of CKLFSF8 mRNA on HL-60 cell line was assayed by RT-PCR; the target gene was transfected into the cells by lipid vector, cell proliferation was determined by MTT assay, while expression of EGFR in HL-60 was determined by immunocytochemical technique. The results indicated that expression of CKLFSF8 existed in HL-60 cells. After transfection, cell proliferation was inhibited (P < 0.05) and the expression of EGFR in HL-60 cells was also discovered to be inhibited (P < 0.05). It is concluded that the proliferation and expression of EGFR in HL-60 cells can be inhibited by transfection of CKLFSF8. The novel chemokine may provide a new approach in the treatment of leukemia.
Cell Proliferation ; Chemokines ; metabolism ; Gene Expression Regulation, Neoplastic ; HL-60 Cells ; Humans ; MARVEL Domain-Containing Proteins ; RNA, Messenger ; metabolism ; Receptor, Epidermal Growth Factor ; metabolism ; Transfection

Cloning, Molecular ; Escherichia coli ; genetics ; Hepacivirus ; genetics ; Humans ; Recombinant Fusion Proteins ; biosynthesis ; genetics ; immunology ; Viral Nonstructural Proteins ; biosynthesis ; genetics ; immunology

The aim of this study was to investigate whether exosomes derived from K562 cells and human monocyte-derived dendritic cells (DCs) transfected with total RNA of K562 cells are capable of inducing antigen-specific cytotoxic T lymphocytes (CTL) responses in vitro. DCs were generated from peripheral blood mononuclear cells (PBMNC) of healthy volunteers in the presence of GM-CSF and IL-4, and then were transfected with K562 RNA by using DOTAP lipofection. Exosomes was extracted from the supernatant of DCs and K562 cells. The T cell were activated to be tumor specific CTL after DCs and exosomes were co-cultured with autologous T cells derived from healthy volunteers' PBMNC. The effect of CTL on K562 cells was detected by MTT assay. The results showed that treatment of T cells with exosomes derived from K562 cells or DCs transfected with total RNA of K562 cells could significantly promote their killing ability on K562 cells as compared with untreated T cells (P < 0.05). The killing ability of T cells treated with exosomes on K562 cells was stronger than on HL-60 cells (P < 0.05). It is concluded that the specific CTL immune response to leukemia cells can be induced by exosomes derived from K562 cells.
Dendritic Cells ; cytology ; immunology ; Endosomes ; immunology ; Exocytosis ; immunology ; Humans ; K562 Cells ; Monocytes ; cytology ; RNA, Neoplasm ; genetics ; immunology ; T-Lymphocytes, Cytotoxic ; immunology ; Transfection

An experimental model of reproducible focal cerebral contusions in rats was made by a free-drop impacting right hemisphere. The expression of fibronectin and its mRNA after cerebral contusion were detected respectively by immunohistochemical staining and in situ hybridization. Results indicated that the expression of fibronectin and its mRNA increased after injury, and there existed a relationship between increased fibronectin and its mRNA and different intervals after brain injury. It is inferred that the expression of fibronectin and its mRNA can be used for timing of brain injuries and distinguishing antemortem and postmortem brain contusions.
Animals ; Brain Injuries/metabolism* ; Fibronectins/biosynthesis* ; Immunohistochemistry ; In Situ Hybridization ; Male ; Postmortem Changes ; RNA, Messenger/biosynthesis* ; Rats ; Rats, Sprague-Dawley ; Time Factors

Objective To establish the national quantity standard of hepatitis B surface antigen according to the world health organization's standard material and prepare, the national liner reference panel for hepatitis B surface antigen. Methods Sera from hepatitis B patients and health blood donors in different areas were collected and detected by domastic HBsAg kits, anti-HBs kits, HBeAg kits, anti-Hbe kits, anti-Hbe kits and anti-HCV,and then confirmed by the kits produced by Abbott, which was approved by WHO. One serum with high concentration of HBsAg was calibrated with the standard sample of WHO. And then it was diluted by 1.5 fold as the liner HBsAg reference panel. Results The HBsAg concentration of one serum was 1226 IU/ml calibrated by 21 independent standardization measurements with 7 kinds of kits. The coefficient of variation of cash calibration were less then 15%. A panel contained 8 serial dilutions was established as the national liner HBsAg reference panel. The permitted range of every dilution was stipulated and the stability of the panel was detected by accelerated test. Conclusions The national quantity standard of hepatitis B surface antigen was established and the national quantitative reference panel for HBsAg which contains eight liner serum was developed.

OBJECTIVETo investigate the effects of dexamethasone on human lung fibroblast cell proliferation, cell cycles, and cell mitogen-activated protein kinases (MAPKs) passway.

METHODSDexamethasone was used at various concentration in culture medium. Cell number was counted using a hemacytometer. Whole cell propidium iodide staining and flow cytometric analysis were performed to determine cellular DNA content. MAPK proteins and activation were tested by Western blot analysis with antibodies to c-Jun N-terminal kinase (JNK), phospho-JNK, extracellular signal-regulated kinase (ERK), phospho-ERK, p38 and phospho-p38.

RESULTS1x10(-7) mol/L and 1x10(-6) mol/L dexamethasone suppressed the proliferation of lung fibroblast cells by 34% and 72%, respectively, than that of control. This suppression was dose-dependant. Dexamethasone suppressed cell cycle with accumulation of cells in G1/G0 stage. It increased from 81.9% to 90.1% compared with that of control. We did not find any apoptosis induced by dexamethasone for lung fibroblast cells. Using Western blot analysis, we found that dexamethasone resulted in decreased activity of ERK, but had no effects on JNK and p38.

CONCLUSIONSDexamethasone may suppresses the proliferation of lung fibroblast cells, which is partly resulted from the facts that it can inhibit ERK activation in MAPK-signaling pathway but has little effect on JNK and p38 pathway. Dexamethasone may not induce lung fibroblast cell apoptosis directly.

Cell Cycle ; drug effects ; Cell Division ; drug effects ; Cells, Cultured ; Depression, Chemical ; Dexamethasone ; pharmacology ; Fibroblasts ; cytology ; Humans ; Lung ; cytology ; MAP Kinase Signaling System ; drug effects ; Mitogen-Activated Protein Kinase Kinases ; drug effects